Abstract
The mechanism of acceleration of lipid peroxide formation in the liver homogenate of vitamin E-deficient mice was investigated. The quantities of unsaturated fatty acid, NADPH, ascorbate and hemo-protein, which have been so far thought to be the main factors of ac-celeration of lipid peroxidation, could not be considered the major reason for acceleration in vitamin E-deficient liver homogenate.
The phenomena resulting from the addition of a surfactant to normal liver homogenate and subcellular fractions resemble those obtained in E-deficient homogenate; (a) Though the rate of lipid peroxidation in E-deficient liver homogenate was 4.5-fold higher than that in normal one, the maximum rate of lipid peroxidation induced by the addition of Tween 80 was only little different in the above two homogenates. (b) Homogenate concentration of normal mouse liver in which maximum acceleration of lipid peroxidation was shown was lower than that of the E-deficient homogenate but shifted towards a higher concentration following the addition of Tween 80. (c) Vitamin E deficiency and the in vitro addition of Tween 80 resulted the decline of aminopyrine oxidation but in the activation of both the NADPH-linked enzymatical lipid peroxi-dation and the ascorbate-linked non-enzymatical one in microsomes and mitochondria.
These results indicate the possibility that the increase in lipid peroxida-tion in E-deficient liver was not a cause but a subsequence of membrane alteration, especially a change in tertiary structure of membrane-bound heme or non-heme iron protein.
